JC virus (JCV), a ubiquitous polyoma virus that commonly infects humans, was first identified as the etiologic agent for the fetal
demyelinating disease,
progressive multifocal leukoencephalopathy. Recently, a number of reports have documented detection of JCV in samples derived from several types of neural as well as non-neural human
tumors. It has been suggested that oncogenicity of JCV depends on a
T antigen having a strict structural homology to the
T antigen of simian virus 40. To clarify whether JCV might have a potential role with regard to
colorectal cancers, we investigated the presence of its genome in a series of cases along with colorectal
adenomas and normal colonic mucosa, targeting
T antigen, VP and agnoprotein by nested polymerase chain reaction and Southern blotting and
T antigen by immunohistochemistry. While VP and agnoprotein were not found in any of the samples examined,
T antigen was detected in 6 of 23
colorectal cancers (26.1%) and 1 of 21
adenomas (4.8%), but none of 20 samples of normal colonic mucosa. No clear and diffuse staining with
anti-T-
antigen antibodies (1:100) could be detected, and there was no correlation with CD20-positive cells, which might have indicated JCV
latent infection of B lymphocytes. Presence of
T antigen did not influence clinicopathological variables, including survival. In one
colonic cancer case positive for
T antigen together with
lymph node metastasis,
DNA extracted from
cancer cells in the lymph node revealed no detection of
T antigen. Our results are in the intermediate position between the high
T antigen rate (81%) in one report and the lack of it (0%) in another focused on
colon cancers. It was concluded that
T antigen might be integrated in
cancer cells in approximately one fourth of Japanese
colon cancer cases without clear and diffuse expression of the
protein, suggesting a possible role in
oncogenesis which might involve a hit-and-run mechanism.